ReviewJournal of cellular and molecular medicine2008
Nogo-A and Nogo-66 receptor in amyotrophic lateral sclerosis.
Review in Journal of cellular and molecular medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Tubular ER dysfunction in neurodegenerative diseases.Neurobiology of disease · 2025Review
- Lateral olfactory tract usher substance (LOTUS), an endogenous Nogo receptor antagonist, ameliorates disease progression in amyotrophic lateral sclerosis model mice.Cell death discovery · 2023Article
- The Role of Clinical Assessment in the Era of Biomarkers.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Sensory Involvement in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2022Review
- Characterization of somatosensory neuron involvement in the SOD1Scientific reports · 2022Article
- The Regulatory Role of Reticulons in Neurodegeneration: Insights Underpinning Therapeutic Potential for Neurodegenerative Diseases.Cellular and molecular neurobiology · 2021Review
- The Skeletal Muscle Emerges as a New Disease Target in Amyotrophic Lateral Sclerosis.Journal of personalized medicine · 2021Review
- The Implication of Reticulons (RTNs) in Neurodegenerative Diseases: From Molecular Mechanisms to Potential Diagnostic and Therapeutic Approaches.International journal of molecular sciences · 2021Review
- Nogo-A regulates myogenesis via interacting with Filamin-C.Cell death discovery · 2021Article
- The rs696880 Polymorphism in the Nogo-A Receptor Gene (Frontiers in aging neuroscience · 2018Article
- RNAi targeting Nogo Receptor enhanced survival and proliferation of murine retinal ganglion cells during N-methyl-D-aspartate-induced optic nerve crush.Oncotarget · 2017Article
- Assessment of Nogo-66 receptor 1 function in vivo after spinal cord injury.Neurosurgery · 2014Article
- The expression patterns of Nogo-A, myelin associated glycoprotein and oligodendrocyte myelin glycoprotein in the retina after ocular hypertension: the expression of myelin proteins in the retina in glaucoma.Neurochemical research · 2011Article
- Serum Nogo-A levels are not elevated in amyotrophic lateral sclerosis patients.Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals · 2009Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nogo/reticulon (RTN)-4 has been strongly implicated as a disease marker for the motor neuron disease amyotrophic lateral sclerosis (ALS). Nogo isoforms, including Nogo-A, are ectopically expressed in the skeletal muscle of ALS mouse models and patients and their levels correlate with the disease severity. The notion of a direct involvement of Nogo-A in ALS aetiology is supported by the findings that Nogo-A deletion in mice reduces muscle denervation and prolongs survival, whereas overexpression of Nogo-A destabilizes motor nerve terminals and promotes denervation. Another intriguing, and somewhat paradoxical, recent finding revealed that binding of the Nogo-66 receptor (NgR) by either agonistic or antagonistic Nogo-66-derived peptides protects against p75 neurotrophin receptor (p75(NTR))-dependent motor neuron death. Ligand binding by NgR could result in subsequent engagement of p75(NTR), and this association could preclude pro-apoptotic signalling by the latter. Understanding the intricate interplay among Nogo isoforms, NgR and p75(NTR) in ALS disease progression may provide important, therapeutically exploitable information.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.